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Involvement of Growth Factor Receptor and Nonreceptor Protein Tyrosine Kinases in Endothelin-1 and Angiotensin II-Induced Signaling Pathways in the Cardiovascular System

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Molecular Defects in Cardiovascular Disease

Abstract

Endothelin-1 (ET-1) and angiotensin II (Ang II) play important roles in maintaining blood pressure and vascular homeostasis, and a heightened activity of these vasoactive peptides are thought to contribute to the development of vascular pathologies, such as hypertension, atherosclerosis, hypertrophy, and restenosis. This is caused by an excessive activation of several growth and proliferative signaling pathways, which include members of the mitogen-activated protein kinase (MAPK) family, as well as the phosphatidylinositol 3-kinase (PI3-K)/protein kinase B (PKB) pathway. ET-1 and Ang II stimulate these pathways through the activation of transmembrane guanine nucleotide-binding protein-coupled receptors (GPCRs). While the activation of these signaling pathways is well elucidated, the upstream elements responsible for ET-1 and Ang II-induced MAPK and PI3-K/PKB activation remain poorly understood. During the last several years, the concept of transactivation of receptor protein tyrosine kinases (PTKs), such as EGFR, IGF-1R, and nonreceptor PTK, in triggering vasoactive peptide-induced signaling events has gained much recognition. As such, in this chapter, we provide an overview of the role of receptor and nonreceptor PTKs in modulating ET-1 and Ang II-induced PI3-K/PKB and MAPK signaling events in vascular smooth muscle cells (VSMC), and their potential implication in vascular pathology.

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Acknowledgments

The work in the authors’ laboratory is supported by funding from the Canadian Institutes of Health Research (CIHR) operating grant number 67037 to A.K.S. G.V. is the recipient of PhD studentships from the Faculty of Medicine, Université de Montréal and the Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM).

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Authors and Affiliations

  1. Laboratory of Cellular Signaling, Montreal Diabetes Research Center, Research Center – Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, Québec, Canada

    George Vardatsikos

  2. Department of Medicine, Université de Montréal, Montreal, Québec, Canada

    George Vardatsikos

  3. Laboratory of Cellular Signaling, Montreal Diabetes Research Center, Research Center – Centre Hospitalier de l’Université de Montréal (CRCHUM), Montréal, Québec, Canada

    Ashok K. Srivastava

  4. Department of Medicine, Université de Montréal, Montréal, Québec, Canada

    Ashok K. Srivastava

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  1. George Vardatsikos
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Correspondence to Ashok K. Srivastava .

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Editors and Affiliations

  1. St. Boniface General Hospital, Research Centre, Institute of Cardiovascular Sciences, Tache Avenue 351, Winnipeg, R2H 2A6, Manitoba, Canada

    Naranjan S. Dhalla

  2. Jikei University School of Medicine, Shibuya-ku, Ebisu 3-31-6, Tokyo, 150-0013, Japan

    Makoto Nagano

  3. Czech Republic, Institute of Physiology, Academy of Sciences of the, Videnska 1083, Prague, 142 20, Czech Republic

    Bohuslav Ostadal

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Vardatsikos, G., Srivastava, A.K. (2011). Involvement of Growth Factor Receptor and Nonreceptor Protein Tyrosine Kinases in Endothelin-1 and Angiotensin II-Induced Signaling Pathways in the Cardiovascular System. In: Dhalla, N., Nagano, M., Ostadal, B. (eds) Molecular Defects in Cardiovascular Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-7130-2_23

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